Effects of electroacupuncture on the ultrastructure and the Nogo-A expressions in the cerebral cortex in rats with cerebral ischemia-reperfusion.
- Author:
Yan-Qui LIANG
1
;
Feng TAN
;
Jie CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Acupuncture Points; Animals; Brain Ischemia; metabolism; pathology; therapy; Cerebral Cortex; metabolism; ultrastructure; Electroacupuncture; Male; Myelin Proteins; metabolism; Nogo Proteins; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; pathology; therapy
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(2):209-213
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effects of electroacupuncture (EA) on the expressions of Nogo-A and the ultrastructure in the cerebral cortex at different time points after the cerebral ischemia-reperfusion in rats.
METHODSOne hundred and thirty male Sprague Dawley (SD) rats were randomly divided into the EA group (n = 30), the sham-EA group (n = 30), the model group (n = 30), the sham-operation group (n = 30), and the blank group (n = 10). The modified ZeaLonga method was used to prepare the left middle cerebral artery occlusion (MCAO) model in the first three groups. After the operation Baihui (DU20) and Dazhui (DU14) were daily needled in the EA group. One inch beside Baihui (DU20) and Dazhui (DU14) were daily needled in the sham-EA group. Rats in the model group were only treated with MCAO ischemia/reperfusion. Rats in the sham-operation group only received surgical wound. No treatment was given to rats in the blank group. The ultrastructures of ischemic cells and the intervention of the Nogo-A expressions were observed using the immunohistochemical staining and the transmission electron microscope 1, 7, and 28 days after EA.
RESULTS(1) In the EA group, the damage of ultrastructures of neurons, gliocytes, and blood brain barrier in the ischemic region was alleviated when compared with that of the sham-EA group and the model group. (2) On the 1st, 7th and 28th day after the cerebral ischemia-reperfusion, the expressions of Nogo-A in the ischemic cortex in the EA group was lower when compared with those in the sham-EA group and the model group at the corresponding time points, showing significant difference (P < 0.05). But there was no statistical difference between the sham-EA group and the model group at the same time point (P > 0.05).
CONCLUSIONThe mechanism of EA for protecting cerebral ischemia/reperfusion might be closely associated with alleviating the damage on the ultrastructures of brain cells, and down-regulating the expressions of Nogo-A.